leukotoxin and Periodontal-Diseases

Recent evidence implicates Actinobacillus actinomycetemcomitans in the etiology of localized juvenile periodontitis. This paper reviews the morphological, biochemical and serological charcteristics of A. actinomycetemcomitans, evidence incriminating it as a periodontopathogen, its importance in human nonoral infections, and virulence factors which may be involved in the pathogenesis of A. actinomycetemcomitans infections. A. actinomycetemcomitans is a non-motile, gram-negative, capnophilic, fermentative coccobacillus which closely resembles several Haemophilus species but which does not require X or V growth factors. The organism has been categorized into 10 biotypes based on the variable fermentation of dextrin, maltose, mannitol, and xylose and into 3 serotypes on the basis of heat stable, cell surface antigens. A. actinomycetemcomitans' primary human ecologic niche is the oral cavity. It is found in dental plaque, in periodontal pockets, and buccal mucosa in up to 36% of the normal population. The organism can apparently seed from these sites to cause severe infections throughout the human body such as brain abscesses and endocarditis. There is a large body of evidence which implicates A. actinomycetemcomitans as an important micro-organism in the etiology of localized juvenile periodontitis including: (1) an increased prevalence of the organism in almost all localized juvenile periodontitis patients and their families compared to other patient groups; (2) the observation that localized juvenile periodontitis patients exhibit elevated antibody levels to A. actinomycetemcomitans in serum, saliva and gingival crevicular fluid; (3) the finding that localized juvenile periodontitis can be successfully treated by eliminating A. actinomycetemcomitans from periodontal pockets; (4) histopathologic investigations showing that A. actinomycetemcomitans invades the gingival connective tissue in localized juvenile periodontitis lesions; (5) the demonstration of several pathogenic products from A. actinomycetemcomitans including factors which may: (a) facilitate its adherence to mucosal surfaces such as capsular polysaccharides; (b) inhibit host defense mechanisms including leukotoxin, a polymorphonuclear leukocyte chemotaxis inhibiting factor, and a lymphocyte suppressing factor (c) cause tissue destruction such as lipopolysaccharide endotoxin, a bone resorption-inducing toxin, acid and alkaline phosphatases, collagenase, a fibroblast inhibiting factor and an epith

Topics: Actinobacillus; Actinobacillus Infections; Adult; Aggressive Periodontitis; Anti-Bacterial Agents; Bacteriological Techniques; Collagen; Endocarditis, Bacterial; Exotoxins; Humans; Infections; Periodontal Diseases; Serotyping

Aggregatibacter actinomycetemcomitans and Fusobacterium nucleatum are strongly associated with periodontitis, and their evaluations are relevant to understand their role in the etiology and progression of periodontal diseases. In this study, the qualitative and quantitative detection of A. actinomycetemcomitans and F. nucleatum, as well as their genetic diversity, were evaluated in individuals with gingivitis, chronic periodontitis and periodontally healthy. In addition, the biotyping, serotyping, and prevalence of the ltx and cdt genes in A. actinomycetemcomitans were also determined. Subgingival biofilms obtained from gingivitis (70), periodontitis (75) and healthy (95) individuals were analyzed by cultures and PCR. Bacterial typing and presence of ltx and cdt genes in A. actinomycetemcomitans were also verified. DNA from A. actinomycetemcomitans and F. nucleatum was detected respectively, in 65.7% and 57.1% of gingivitis, 80% and 68% of periodontitis, and 57.8% and 37.8% of healthy. A. actinomycetemcomitans from gingivitis were biotypes I, II, IV, V, and X, and serotypes a, c, and e. In periodontitis, biotypes II, VI, and X, and serotypes a, b, and c were found. In healthy subjects, biotypes II and X, and serotypes b and c were found. The LTX and ltxA were observed in strains from gingivitis and periodontitis pockets. Subsequently, our data also showed no direct relationship between ltxA gene expression and leukotoxin gene 530-bp presence. On the other hand, cdt gene predominated during the inflammatory disease process. Our results strongly support a role of A. actinomycetemcomitans and F. nucleatum in advanced stage of periodontal disease.

Topics: Adult; Aggregatibacter actinomycetemcomitans; Bacterial Toxins; Cross-Sectional Studies; Exotoxins; Female; Fusobacterium nucleatum; Genotype; Humans; Male; Middle Aged; Periodontal Diseases; Young Adult

Aggregatibacter actinomycetemcomitans is a Gram-negative bacteria that has gained wide recognition for its causative role in the development of various immune diseases, which includes localized aggressive periodontitis. Its ability to evade host defense mechanisms is mediated by the secretion of leukotoxin (LtxA), which induces death of white blood cells (leukocytes) by specific binding to their surface-expressed leukocyte function-associated receptor (LFA-1) in its active state. Therapeutic compounds that interfere with this pathogenic process and abrogate A. actinomycetemcomitans virulence have been reported in literature. These include doxycycline, and more recently phytochemical compounds such as hamamelitanin, resveratrol, naringin, and quercetin. However, the question remains how do they work? Therefore, with the aid of computational tools, we explore the molecular mechanisms by which they possibly elicit their therapeutic functions. Molecular mechanics Poisson/Boltzmann surface area analyses revealed that these compounds bind favorably to active LFA-1 with high affinity and considerable stability, indicative of their ability to occupy the LtxA binding site (LBS) and prevent LtxA binding. The conformational transition of open LFA-1 to its closed state further describe the mechanistic activity of these compounds. In addition to notable reductions in structural mobility and flexibility, the burial of surface-exposed interactive side chains at the LBS was observed, an occurrence that could alter the complementary binding of LtxA. It is also important to mention that these occurrences were induced more prominently by the phytochemicals. We believe that these findings will enhance the scope of drug design and discovery for potent LtxA antagonists with improved activities and therapeutic efficacies in the treatment of virulent A. actinomycetemcomitans diseases.

Topics: Animals; Datasets as Topic; Exotoxins; Humans; Periodontal Diseases; Protein Binding; Protein Structure, Secondary; Thermodynamics

The periodontal pathogen Aggregatibacter actinomycetemcomitans is known to elicit a systemic immune response in the infected host, and occasionally causes non-oral infections. Detailed information on its immunopathological responses and the involvement of bacterial virulence factors remains to be elucidated. The aim of this study was to assess the systemic immune response to A. actinomycetemcomitans oral infection. We used an animal model that simulates systemic dissemination of the bacteria by injecting live wild-type (WT) D7S-1 and a double knockout mutant of leukotoxin and cytolethal distending toxin (ΔltxΔcdt) A. actinomycetemcomitans strains in rat oral mucosa. Draining lymph nodes were examined for regulatory T (Treg) and T helper type 17 (Th17) cell subsets and their associated mediators. An increase in the proportion of Th17 cells and a decrease in Treg cells over the experimental period of 3 weeks were similarly observed for rats challenged with WT and ΔltxΔcdt. Significant upregulation and downregulation of proinflammatory cytokines in the Th17 gene pathway was noted, as well as several qualitative differences between WT and ΔltxΔcdt. Furthermore, we observed differential fold regulation in key genes associated with a proinflammatory response in ΔltxΔcdt-inoculated rats relative to D7S-1 group. This suggests that although the knockout of these two virulence factors (ΔltxΔcdt) may suppress certain proinflammatory genes, it causes similar over-expression of other genes compared with D7S-1, indicating a common factor that still remains in the pathogenicity of A. actinomycetemcomitans.

Topics: Aggregatibacter actinomycetemcomitans; Animals; Bacterial Toxins; Biofilms; Cytokines; Exotoxins; Female; Gene Expression; Gene Knockout Techniques; Immunity; Lymph Nodes; Models, Animal; Periodontal Diseases; Rats; Rats, Sprague-Dawley; Receptors, Cytokine; T-Lymphocytes, Regulatory; Th17 Cells; Virulence; Virulence Factors

Our aim was to explore the effects of Cytolethal Distending toxin (Cdt) in a well established rat model of periodontal disease where leukotoxin (LtxA) was thought to have no known effect. In vitro studies, were used to assess CdtB activity using Aa Leukotoxin as a negative control. These studies showed that both CdtB and LtxA (unexpectedly) exerted significant effects on CD4(+) T cells. As a result we decided to compare the effects of these two prominent Aa virulence factors on bone loss using our rat model of Aa-induced periodontitis. In this model, Aa strains, mutant in cdtB and ltxA, were compared to their parent non-mutant strains and evaluated for colonization, antibody response to Aa, bone loss and disease. We found that bone loss/disease caused by the ltxA mutant strain, in which cdtB was expressed, was significantly less (p<0.05) than that due to the wild type strain. On the other hand, the disease caused by cdtB mutant strain, in which ltxA was expressed, was not significantly different from the wild type strain. This data indicates that Aa LtxA exerts a greater effect on bone loss than Cdt in this rat model of periodontal disease and supports the utility of this model to dissect specific virulence factors as they relate to immunopathology in studies of Aa-induced disease.

Topics: Aggregatibacter actinomycetemcomitans; Animals; Bacterial Toxins; CD4-Positive T-Lymphocytes; Cell Proliferation; Colony Count, Microbial; Disease Models, Animal; Exotoxins; Male; Mutation; Pasteurellaceae Infections; Periodontal Diseases; Rats; Rats, Sprague-Dawley; Virulence

The aim of our study is to describe a fast molecular method, able to distinguish and quantize the two different genotypes (652 and JP2) of an important periodontal pathogen: Actinobacillus actinomycetemcomitans. The two genotypes show differences in the expression of an important pathogenic factor: the leukotoxin (ltx). In order to evidence this, we performed a real time PCR procedure on the ltx operon, able to recognize Aa clinical isolates with different leukotoxic potentials.. The specificity of the method was confirmed in subgingival plaque and saliva specimens collected from eighty-one Italian (Sardinian) subjects with a mean age of 43.9, fifty five (68 %) of whom had various clinical forms of periodontal disease.. This procedure showed a good sensitivity and a high linear dynamic range of quantization (10(7)-10(2) cells/ml) for all genotypes and a good correlation factor (R2 = 0.97-0.98). Compared with traditional cultural methods, this real time PCR procedure is more sensitive; in fact in two subgingival plaque and two positive saliva specimens Aa was only detected with the molecular method.. A low number of Sardinian patients was found positive for Aa infections in the oral cavity, (just 10 positive periodontal cases out of 81 and two of these were also saliva positive). The highly leukotoxic JP2 strain was the most representative (60 % of the positive specimens); the samples from periodontal pockets and from saliva showed some ltx genotype for the same patient. Our experience suggests that this approach is suitable for a rapid and complete laboratory diagnosis for Aa infection.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Aggregatibacter actinomycetemcomitans; Benzothiazoles; Child; Dental Plaque; Diamines; Exotoxins; Female; Genotype; Humans; Male; Middle Aged; Organic Chemicals; Periodontal Diseases; Polymerase Chain Reaction; Quinolines; Saliva; Sensitivity and Specificity

A high odds ratio has been reported for hyperlipidemia and periodontal diseases in humans, and the severity of periodontitis seems to correlate with the hyperlipidemic status of the patients. Early studies indicated that the lipoprotein-containing fraction of the serum enhances the leukotoxic activity of the periodontopathogen Actinobacillus actinomycetemcomitans against human polymorphonuclear leukocytes (PMNL). The protease inhibitors of normal serum account for this enhancement, while delipidated serum has no effect on the leukotoxin-dependent PMNL cytolysis. No information exists for the effect of serum lipoproteins or hyperlipidemic serum. The aim of this study was to evaluate the role of serum lipoproteins in the interaction of the leukotoxin of A. actinomycetemcomitans with human PMNL. Purified leukotoxin was mixed with human PMNL prepared from venous blood of healthy subjects and various varying amounts of hyperlipidemic or delipidated serum, or purified serum lipoproteins. The cytolytic activity of leukotoxin was determined by activity of the cytosol enzyme lactate dehydrogenase released from injured PMNL. The degranulating activity of the toxin was measured through the release of the granule components elastase and lactoferrin. Normal human serum without leukotoxin-neutralizing antibodies caused a 4-fold enhancement of the leukotoxic activity when present at concentrations of 5-10% in the reaction mixture. Serum lipoproteins had no effect when added at concentrations that occur normally in serum. At high concentrations, purified low density and very low-density lipoproteins increased the leukotoxicity of the mixture. Nevertheless, hyperlipidemic serum prepared from a normal serum by the addition of autologous lipoproteins had no influence on the leukotoxin-caused cytolysis compared to the normal serum. Pre-incubation of PMNL for 1 h in hyperlipidemic or delipidated serum had no effect on the leukotoxin-induced degranulation of PMNL. The results indicate that the cytotoxic interactions of A. actinomycetemcomitans leukotoxin against human PMNL are not influenced by the presence of serum lipoproteins.

Topics: Aggregatibacter actinomycetemcomitans; Comorbidity; Coronary Disease; Cytoplasmic Granules; Disease Susceptibility; Dose-Response Relationship, Drug; Exotoxins; Humans; Hyperlipidemias; L-Lactate Dehydrogenase; Lactoferrin; Leukocyte Elastase; Lipoproteins; Neutrophils; Periodontal Diseases

The aim of the present study was to investigate the intraoral distribution of Actinobacillus actinomycetemcomitans in young adults with minor signs of periodontal disease but harboring the organisms in the oral cavity. 17 healthy volunteers, 20 to 27 years of age, participated. Samples from mucosal surfaces of the oro-pharyngeal cavity and saliva (n = 221) as well as subgingival plaque from every tooth (n =477) were selectively cultivated for A. actinomycetemcomitans. Species identity and presence of the leukotoxin encoding gene, ltxA, were checked by multiplex polymerase chain reaction. Moreover, the leukotoxin promoter region was analyzed. No isolate harbored a 530 bp deletion in the promoter region of the leukotoxin gene, signaling minimally toxic strains. 42.1 +/- 30.4% extracrevicular and 34.4 +/- 29.5% subgingival samples were culture-positive. In extracrevicular samples, the organism could easily be recovered from cheek mucosa (62%), saliva (59%) and the palatal tonsils (41%). Mean log-transformed numbers of A. actinomycetecomitans colony forming units (CFU/ml) in culture-positive material ranged between 1.8 from the hard palate and 2.3 from 10 microl saliva. The highest prevalence in subgingival plaque was observed at maxillary 3rd molars (55%) followed by maxillary lateral incisors (50%) and mandibular 3rd molars (41%). Mean log-transformed counts of CFU/ml ranged between 2.2 at maxillary 3rd molars and 3.4 at upper central incisors. When adjusted for jaw, site and tooth type, the odds of isolating higher numbers of the organism were increased with every mm probing depth by a factor of 1.35 (p <0.05). The odds ratio for bleeding on probing was 1.38. Thus, in this young adult population with minor periodontal disease, A. actinomyetemcomitans was mainly associated with some deviation from gingival health. Of concern might be a minority of subjects (29%) with an extremely wide distribution of the organism in the oral cavity.

Topics: Adolescent; Adult; Aggregatibacter actinomycetemcomitans; Bacterial Toxins; Base Pairing; Colony Count, Microbial; Dental Plaque; Exotoxins; Female; Gingiva; Gingival Hemorrhage; Humans; Incisor; Male; Molar, Third; Mouth; Mouth Mucosa; Odds Ratio; Oropharynx; Palatine Tonsil; Periodontal Diseases; Polymerase Chain Reaction; Prevalence; Promoter Regions, Genetic; Saliva; Sequence Deletion; Statistics as Topic; Tongue

Actinobacillus actinomycetemcomitans strains showing a 530-bp deletion in the promoter region of the leukotoxin gene operon elaborate high amounts of leukotoxin that may play a role in the pathogenesis of periodontal disease. This study used polymerase chain reaction detection to determine the occurrence of the 530-bp deletion in 94 A. actinomycetemcomitans strains from individuals of various ethnic backgrounds. Eleven blacks and one Hispanic subject but no Caucasian or Asian subjects showed the 530-bp deletion in the leukotoxin promoter region, suggesting that the deletion is mainly a characteristic of individuals of African descent. A. actinomycetemcomitans strains exhibiting a deletion in the leukotoxin promoter region occurred both in individuals having severe periodontitis and in adolescents revealing no evidence of destructive periodontal disease.

Topics: Actinobacillus Infections; Adolescent; Adult; Aggregatibacter actinomycetemcomitans; Asian People; Bacterial Toxins; Base Pairing; Black People; Cytotoxins; Ethnicity; Exotoxins; Gene Deletion; Gene Frequency; Hispanic or Latino; Humans; Operon; Periodontal Diseases; Periodontitis; Polymerase Chain Reaction; Promoter Regions, Genetic; White People

Actinobacillus actinomycetemcomitans, a Gram-negative periodontopathic bacterium, produces a leukotoxin belonging to the RTX family. The production of leukotoxin varies greatly among different strains of this species. In this paper the effects of growth rate and bicarbonate on the leukotoxin production by a toxin-production-variable strain (301-b) during growth in a chemostat were examined. When the bacterium was grown in anaerobic fructose-limited chemostat cultures (pH 7.0 and 37 degrees C) at dilution rates (D) ranging from 0.04 to 0.20 h-1 in the absence and presence of 10 mM bicarbonate, it produced leukotoxin as a cluster of two polypeptides (M(r) 113,000 and 120,000) and complexed with nucleic acids on the bacterial cell surface. The relationship between leukotoxin production and specific growth rate was analysed by plotting the specific rate of leukotoxin production [qLT, in microgram (mg dry wt)-1 h-1] against D. The plots were approximated to the linear relationships qLT = 2.7D-0.058 and qLT = 9.3D-0.407 without and with bicarbonate, respectively. These relationships suggest that the apparent leukotoxin production is a result of both growth-rate-dependent production and growth-rate-independent decomposition. The cellular leukotoxin level was also followed after the change from chemostat to batch culture in the same fermenter. In batch culture leukotoxin production stopped immediately and the cellular toxin level rapidly decreased, suggesting toxin decomposition. From the slopes of the approximated linear relationships between qLT and D, a theoretical maximum leukotoxin yield (YLT) was estimated as 2.7 and 9.3 micrograms (mg dry wt)-1 in the absence and presence of 10 mM bicarbonate, respectively. The increased YLT value in the cultures containing bicarbonate indicated that the addition stimulated the efficiency of leukotoxin synthesis up to about threefold. Further increases of bicarbonate concentration to between 20 and 40 mM had no effect on the total leukotoxin production, but the amount of extracellular leukotoxin increased with higher bicarbonate concentrations.

Topics: Actinobacillus Infections; Aggregatibacter actinomycetemcomitans; Amino Acid Sequence; Bacterial Toxins; Bacteriological Techniques; Bicarbonates; Culture Media; Exotoxins; Humans; Kinetics; Molecular Sequence Data; Molecular Weight; Periodontal Diseases; Virulence

Eighteen (18) members of an extended family in which numerous individuals have Papillon-Lefèvre syndrome (PLS) were examined. In all, 6 affected members and 12 non-affected members were included. All patients underwent a clinical examination which, in the dentate persons, included plaque index, bleeding on probing, probing depth, and periodontal attachment loss and a set of full mouth periapical x-rays. Subgingival bacterial samples were also collected from 2 teeth in the dentate patients for cultures and identification of Actinobacillus actinomycetemcomitans. Serum samples were collected from all participants and assayed for antileukotoxin antibodies. The results indicate that there is a high prevalence of leukotoxic strains of A. actinomycetemcomitans in persons suffering from PLS, as well as in unaffected family members. The ubiquitous presence of A. actinomycetemcomitans in the family units suggests a close association between A. actinomycetemcomitans and the periodontal disease associated with the syndrome; it also suggests that A. actinomycetemcomitans by itself is not sufficient for the expression of periodontal disease and that other factors, some of which must be genetic, are necessary for lesion development.

Topics: Adolescent; Adult; Aggregatibacter actinomycetemcomitans; Antibodies, Bacterial; Bacteria; Bacterial Toxins; Child, Preschool; Colony Count, Microbial; Cytotoxins; Dental Plaque Index; Exotoxins; Female; Gingival Hemorrhage; Humans; Male; Middle Aged; Papillon-Lefevre Disease; Periodontal Attachment Loss; Periodontal Diseases; Periodontal Pocket

Actinobacillus actinomycetemcomitans (A.a.) can produce a potent leukotoxin that is thought to be involved in evasion of the host immune response. In order to understand the role of A.a. and its leukotoxin in the initiation and progression of periodontal disease, it is important determine how the expression of A.a. virulence factors might be regulated by the local periodontal micro-environment. To facilitate the measurement of leukotoxin levels, a leukotoxin-beta-galactosidase gene fusion was constructed and recombined into the chromosome of A.a. strain JP2 at the leukotoxin locus. The resulting strain, AAM17, produces beta-galactosidase under control of the leukotoxin promoter. It also produces leukotoxin, since integration of the gene fusion into the chromosome was designed to produce a duplication of the leukotoxin gene. This strain was used to measure the change in leukotoxin level in response to alterations in two environmental signals: iron concentration and oxygen tension. When AAM17 was grown in iron-limited media that did not alter growth rate but did increase the levels of other iron-regulated proteins, the levels of the leukotoxin-beta-galactosidase were similar to those found in AAM17 grown in iron-replete media. These results were confirmed in strains AAM17 and JP2 by leukotoxicity assays and RNA blots. Aerobic growth of AAM17 resulted in a three-fold decrease in leukotoxin beta-galactosidase activity compared with anaerobically grown cells. These results indicate that the A.a. leukotoxin is regulated by some of the environmental signals that may vary in the gingival crevice.

Topics: Aggregatibacter actinomycetemcomitans; Bacterial Toxins; beta-Galactosidase; Cloning, Molecular; Cytotoxins; Exotoxins; Gene Expression Regulation, Bacterial; Genes, Bacterial; Humans; Immunosuppressive Agents; Iron; Oxygen; Periodontal Diseases; Plasmids; Restriction Mapping

Strains of A. actinomycetemcomitans (A.a) from juvenile periodontitis patients (JP), adult periodontitis patients (AP), and 14-yr-old healthy children were tested for the correlation between leukotoxin activity and the number of outer membranous vesicles measured in electron micrographs. To determine the potential for connective tissue destruction following the interaction of polymorphonuclear leukocytes (PMN) with the bacteria, the lysosomal release of neutrophil elastase was assessed. The highest potential to kill leukocytes and to release lysosomal elastase from them was observed in the strains isolated from JP patients. No correlation existed between leukotoxic activity and the number of outer membranous vesicles per bacterium when the data from A.a. strains from all sources were combined. Furthermore, no significant differences were found between the numbers of outer membranous vesicles in the three groups tested. The only significant correlation between the number of vesicles and leukotoxicity was found in the A.a. strains derived from the mouths of healthy children.

Topics: Actinobacillus; Adolescent; Adult; Aggressive Periodontitis; Bacterial Toxins; Cell Membrane; Exotoxins; Humans; Microscopy, Electron; Middle Aged; Neutrophils; Pancreatic Elastase; Periodontal Diseases; Periodontitis

The leukotoxin of Actinobacillus actinomycetemcomitans has been implicated in the pathogenesis of inflammatory periodontal disease. We examined a potential mechanism for detoxification of this microbial product by the neutrophil myeloperoxidase system. Exposure to myeloperoxidase, H2O2, and a halide resulted in marked inactivation of leukotoxin, an effect which required each component of the myeloperoxidase system. Toxin inactivation was blocked by agents which inhibit heme enzymes (azide, cyanide) or degrade H2O2 (catalase). Reagent H2O2 could be replaced by the peroxide-generating enzyme system glucose oxidase plus glucose. The latter system, in fact, was more potent than reagent H2O2 in terms of the capacity to inactivate high concentrations of toxin. Toxin inactivation was complete within 1 to 2 min at 37 degrees C. These observations suggest a possible role for oxidative inactivation of leukotoxin by secretory products of neutrophils.

Topics: Actinobacillus; Child; Exotoxins; Humans; Hydrogen Peroxide; Male; Neutrophils; Oxidation-Reduction; Periodontal Diseases; Peroxidase

Topics: Actinobacillus; Adhesiveness; Bacteroides; Capnocytophaga; Chemotaxis, Leukocyte; Cytophagaceae; Dental Plaque; Ecology; Exotoxins; Humans; Immunoglobulins; Periodontal Diseases; Phagocytosis; Virulence

Human serum antibody responses to antigens from a suspected oral pathogen, Actinobacillus actinomycetemcomitans (Aa), were studied. IgG and IgM isotype antibodies to four antigen preparations, sonicate antigen (SA), leukotoxin (LT), group carbohydrate (LG), and lipopolysaccharide (LPS), were determined using an ELISA. An ELISA inhibition technique was developed to show that human serum antibodies reacting with the LT, LG, or LPS materials were binding to different antigenic moieties in each preparation. Cross-sectional studies of serum IgG antibodies showed that patients with localized juvenile periodontitis (LJP) had a greater frequency of occurrence and a higher level of antibodies to the SA (82%), LT (70%), and LG (62%) antigens compared to all other diseased (11-46%) or normal (4-13%) groups. Serum IgM antibodies to LPS were increased in LJP, generalized juvenile periodontitis, and adult periodontitis patients compared to all other groups. Therefore, while both IgG and IgM antibodies were found against various Aa antigens, the detection of IgG antibodies was most clearly associated with the specific disease classification of LJP. Blocking studies suggested that the human serum responses were specific for the Aa antigens and that the LT, LG, and LPS comprise major antigenic determinants on the organisms to which human serum antibody reacts.

Topics: Actinobacillus; Actinobacillus Infections; Adolescent; Adult; Aggressive Periodontitis; Antibodies, Bacterial; Antigen-Antibody Reactions; Antigens, Bacterial; Binding Sites, Antibody; Binding, Competitive; Enzyme-Linked Immunosorbent Assay; Epitopes; Exotoxins; Humans; Middle Aged; Periodontal Diseases; Polysaccharides, Bacterial